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MBBS IV - Junior Clerkship WCS > JC26 (Medicine) - Headache and Neuralgia > Flashcards

JC26 (Medicine) - Headache and Neuralgia Flashcards

1
Q

Differentiate primary and secondary headache

A

□ Primary headache (~90%): benign headaches that does NOT arise from structural brain lesions
□ Secondary headache: headache occurs as a symptom of an underlying disease

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2
Q

5 most common types of headaches

A

Tension type headache (50-70%)

Migraine (10-15%)

Medication overuse

Cluster headache

Raised ICP

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3
Q

Pathophysiology of headache (pain sensitive structures)

A

Headache results from pressure, traction, displacement or inflammation of nociceptors in head

Intracranial pain-sensitive structures:
□ Vessels: venous sinuses, cortical veins, basal arteries
□ Dura

Extracranial pain-sensitive structures:
□ Scalp: vessels and muscles
□ Orbit
□ Cavities: oral, nasal, paranasal sinuses
□ Ear: external and middle ear

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4
Q

List 4 primary headaches

A

Tension-type headaches

Migraine

Cluster headache

Headache associated with specific activities

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5
Q

List secondary causes of headaches

A

Raised ICP

Meningitis

Temporal arteritis

Subarachnoid hemorrhage

Cervical spondylosis

Others:

  • Vascular: carotid/vertebral dissection, hypertensive crisis, vasculitis
  • CSF: CSF hypotension, post-LP headache
  • Other cranial structures: acute glaucoma, head trauma, neuralgia (post-herpetic, trigeminal, occipital)
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6
Q

Features of Tension-type headache

Location, character, associated symptoms, temporal course, relieving/ exacerbating factor

A
  • Bilateral, generalized, radiate forwards from occipital region
  • Band-like tightness lasting for hours to weeks, recur often
  • No associated symptoms, pt can carry on with activities

Time course: last for hours to days or even months → May be episodic or chronic (persist over years)

  • Wax and wane, worse on touching scalp and worse in later part of day
  • Can be associated with anxiety/depression/ stress
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7
Q

Tension-type headache

  • Pathophysiology
  • Treatment
A

Pathophysiology: incompletely understood
□ A/w stress, anxiety and underlying depression
□ Muscular in origin: likely a misinterpretation of sensory afferents from epicranial muscles as pain

Treatment:

Short-term (abortive): NSAIDs, COX-2 inhibitor, paracetamol, combination

Long-term (prophylactic):
→ Pharmacological: amitriptylline
→ Nonpharmacological: behavioural therapy

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8
Q

Features of migraine

Location, character, associated symptoms, temporal course, relieving/ exacerbating factor

A
  • Unilateral severe and Pulsatile/ Throbbing pain for 4-72h
  • 20% preceded by aura (99% visual, 31% sensory, 18% aphasic, 6% motor)
  • Associated with photophobia, phonophobia, nausea/vomiting
  • Debilitating (worsens by movement) → lies in a quiet, dark room
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9
Q

Features of Cluster headache

Location, character, associated symptoms, temporal course, relieving/ exacerbating factor

A
  • Severe, unilateral periorbital pain for 15-180 min
  • Strikingly periodic – begin at same hour for consecutive days over weeks
  • Associated with autonomic features eg. unilateral lacrimation, nasal congestion, conjunctival injection, Horner’s syndrome (~30-50%)
  • highly agitated during attacks
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10
Q

Features of Headache due to Raised ICP

Location, character, associated symptoms, temporal course, relieving/ exacerbating factor

A
  • Generalized headache, worse in morning
  • Associated with drowsiness, LOC or nausea/vomiting
  • Often worsen with coughing and sneezing and relieved with vomiting
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11
Q

Features of Headache due to Meningitis

Location, character, associated symptoms, temporal course, relieving/ exacerbating factor

A
  • Generalized headache with neck stiffness of gradual onset/ meningism
  • Associated with photophobia, ↓consciousness and fever
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12
Q

Features of Headache due to Temporal arteritis

Location, character, associated symptoms, temporal course, relieving/ exacerbating factor

A
  • Persistent unil/bil temporal headache in pt >50y/o
  • Associated with temporal tenderness, jaw claudication, diplopia or amaurosis fugax

Jaw claudication - pain in proximal jaw near TMJ after brief chewing of tough food

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13
Q

Features of Headache due to SAH

Location, character, associated symptoms, temporal course, relieving/ exacerbating factor

A
  • Thunderclap (worst) headache with often dramatic onset
  • Initially localized (often occipital) but becomes generalized
  • Commonly occurs on physical exertion, straining and sexual excitement
  • Associated with meningism (late, after 6h) ± LOC
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14
Q

Features of Headache due to Cervical spondylosis

Location, character, associated symptoms

A
  • Commonly over occipital region (supplied by upper cervical roots)
  • Can be a/w neck stiffness (less limited to flexion/extension) or pain
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15
Q

7 questions to characterize headache

A

Characterize the headache:

1) New onset or chronic?
2) Prodrome/precipitation

3) Quality
4) Region

5) Severity
6) Temporal course: acute vs subacute vs chronic
7) Associating symptoms

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16
Q

Ddx types of headache with bilateral vs unilateral involvement, ocular or facial involvment

A

→ Bilateral (TTH, ↑ICP, …) vs unilateral (migraine, cluster, temporal arteritis, trigeminal)
→ Ocular: ocular diseases (eg. acute glaucoma), trigeminal autonomic cephalalgias (TACs), lesions at apex of orbit or cavernous sinus (rare)
→ Facial: trigeminal neuralgia, herpes zoster, post-herpetic neuralgia, dental/TMJ diseases, sinusitis

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17
Q

Red flag signs of severe secondary causes of headache (5)

A
  1. Systemic upset (constitutional symptoms): CNS infection, Neoplasia, Vasculitis
  2. Neurological S/S: Intracranial pathologies
  3. New, Sudden onset: Temporal arteritis, SAH, Anneurysms, Dissections, Hypertensive crises, Acute optic neuritis, acute glaucoma, hydrocephalus
  4. Associated symptoms: trauma (haematoma), vomiting (ICP), Rash (meningococcus), Visual (glaucoma)
  5. Progression or Persistent despite treatment
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18
Q

Primary headaches

  • Compare onset and duration between Migraine, Tension and Cluster headache
A

Migraine: Gradual onset, crescendo; 4-72 hours

Tension: Gradual onset, wax-and-wane; 30min – 7d

Cluster: Rapid onset; 15min – 3h

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19
Q

Primary headaches

Compare triggers, quality and associated symptoms

A

Migraine:

  • Trigger: Premenstrual, stress, exercise
  • Quality: Unilateral pulsating, moderate to severe, Debilitating (worsen by movement)
  • Nausea/vomiting, Photophobia, phonophobia, Preceded by aura

Tension:

  • Trigger: emotions, stress
  • Bilateral band-like tightness
  • No associated symptoms

Cluster

  • Trigger: Alcohol, HTN
  • Severe unilateral periorbital pain, deep and piercing, restless
  • Ipsilateral autonomic features ((lacrimation, nasal congestion, conjunctival injection, Horner’s)
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20
Q

First line investigations for headache

A

P/E: Full neurological exam + H&N exam (skull, C-spine, teeth, ENT, sinuses, eyes) + BP

Investigations: for suspected serious secondary cause:

  • CBC, L/RFT for systemic disease
  • ESR
  • Plain XR e.g. CXR
  • CT/MRI brain (neurological deficits or seizures)
  • Vascular imaging
  • LP CSF analysis (infective or infiltrative)
  • ENT evaluation
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21
Q

Management of migraine

Triggers, abortive Tx and Prophylatic Tx

A
22
Q

Management of Tension type headache

Triggers, abortive Tx and Prophylatic Tx

A
23
Q

Management of Cluster headache

Triggers, abortive Tx and Prophylatic Tx

A
24
Q

Causes of acute headache (9)

A
  1. SAH
  2. Primary heachache: Migraine, Cluster headache
  3. Glaucoma
  4. Arterial dissection: carotid, vertebral
  5. Retrobulbar neuritis
  6. Trauma
  7. Drugs/ toxins
  8. Hydrocephalus
  9. Infection: meningitis/ encephalitis, sinusitis
25
Q

Causes of subacute headache (7)

A
  1. Infection: e.g. chronic meningitis, TB, brain abscess
  2. Intracranial tumor
  3. Chronic subdural haematoma
  4. Hydrocephalus
  5. Idiopathic intracranial hypertension
  6. Temporal arteritis
  7. Intracranial hypotension
26
Q

Causes of chronic headache (6)

A
  1. Tension-type headache
  2. Transformed migraine
  3. Medication overuse headache
  4. Ocular eye strain/ Refractive error
  5. Drugs/ toxins (e.g. vasodilators)
  6. Cervical spondylosis
27
Q

Migraine

  • Frequency for clinical Dx
  • Clinical subtypes
A

Definition: migraine patient defined as
□ ≥2 attacks with aura
□ ≥5 attacks without aura

Types:
□ Migraine with aura (20%): with a warning of visual, sensory or motor type followed by headache
□ Migraine without aura (80%): without aura symptoms
□ Mixed: Up to 33%

28
Q

Migraine pathophysiology

A

Pathophysiology: still unclear

□ Cortical spreading depression (CSD): dysfunctional ion channels → spreading front of cortical depolarization followed by hyperpolarization → ‘aura’ symptoms

□ Neurogenic inflammation: CSD → stimulation of trigeminal nerve endings at cranial vessels → nociceptive neurones on dural blood vessels release plasma proteins and pain neurotransmitters → ‘neurogenic inflammation’ with vasodilatation

□ Pain due to activation of nociceptors and central pain sensitization (∵dysfunction of BS pathways that normally modulate sensory input, eg. dorsal raphe nucleus, locus ceruleus…)

29
Q

Migraine

Temporal Phases and associated features

A

Typical course of migraine:
□ Prodrome (77%): preceding mental and mood fluctuations, fatigue or autonomic symptoms for 24-48h

□ Aura: gradual development of transient focal neurological symptoms; develop over 4-60min before/ during headache
□ Headache: moderate-severe unilateral or bilateral pulsating headache for 4-72h

□ Postdrome: hangover-like state w/ listlessness + sudden head mov’t trigger headache for up to 24h

30
Q

Describe different types of migraine aura

A

Visual (99%):

  • Scotoma (-ve): gradually spreading visual defect, often bordered by fortification spectra
  • Fortification spectra (+ve): shimmering, silvery zig-zag lines that march across visual fields

Sensory: (31%): tingling (+ve) followed by numbness (-ve) spreading from one part of the body to another

Aphasic (18%): transient speech disturbance due to dominant hemisphere involvement

Motor (6%): hemiplegic aura

31
Q

Complications of migraines

A
  1. Chronic migraine if ≥15d/mo for >3mo w/o medication overuse
  2. Status migrainosus: debilitating migraine attack lasting for >72h
  3. Persistent aura w/o infarction: if aura lasts for >1w
  4. Migrainous infarction: aura symptoms lasting for >1h + ischaemic infarct on CT/MRI
  5. Migraine-triggered seizure: epileptic seizure occur during or ≤1h of aura
32
Q

Describe one hereditary primary headache

A

Familial hemiplegic migraine (FHM):
□ Cause: mutations in VGCC α1 subunits (FHM1) or Na+/K+/ATPase α2 subunit (FHM2)

□ Pathophysiology: changes in ion transport → hyper neuronal excitability → susceptibility to cortical spreading depression

33
Q

Triggers of migraine

A

→ Dietary: alcohol, chocolate, tyramine-containing (eg. dairy products), starvation, caffeine
→ Hormonal: often premenstrual or related to OCP (fluctuation in oestrogen)
→ Emotional: stress, anger, excitement
→ Others: change in sleep, irregular meals, certain drugs, smoking, fluorescent lights,
weather

34
Q

Management of acute migraine attack

A

simple analgesics for mild attacks, migraine-specific agents for severe attacks

Simple analgesics: aspirin, paracetamol, NSAIDs, combination
D2-blocker anti-emetic (↓nausea/vomiting + ↓headache): metoclopramide, domperidone

Triptans for severe headache: sumatriptan (oral, subcutaneous, nasal), naratriptan (PO), zolmitriptan (PO)

Ergotamine (also 5HT1 agonist like Triptan)

35
Q

Triptans

  • Indication
  • MoA
  • S/E
  • C/I
A
  • Indication: Severe migraine headache
  • MoA: 5HT1 agonist → vasoconstriction, peripheral neuronal inhibition, ↓trigeminal neurotransmission
  • S/E: dizziness, somnolence, asthenia, nausea
  • C/I: IHD, stroke, CAD, uncontrolled HTN
36
Q

Ergotamine

  • Indication
  • MoA
  • S/E
  • C/I
A
  • Indication: Severe migraine headache
  • MoA: 5HT1 agonist → vasoconstriction, ↓trigeminal neurotransmission
  • S/E: vascular events (sustained generalized vasoconstriction), high risk of overuse syndrome and rebound headache
  • C/I: IHD, thyrotoxic heart disease, PVD, uncontrolled HTN
37
Q

Prophylactic drugs for recurrent migraine

  • Indication
  • Drug types
A
  • Indication
  • Attacks weekly or >2 times a month
  • Attacks less often but very prolonged and debilitating
  • Drug types
  • Prophylactic NSAIDs in menstrual or orgasmic migraine
  • Antihypertensives: β-blockers, CCB
  • Antidepressants: amitriptyline, venlafaxine
  • Anticonvulsants: topiramate, valproate
  • CGRP antagonists, eg. erenumab, fremanezumab, galceanezumab
  • Others: pizotifen (5HT2 blocker), botox injections around H&N q12w (if refractory)
38
Q

Precautions of using analgesics for migraine attacks

A
  • Limit to 2-3d/week → Limit medication overuse headache
  • Keep headache diary → monitor for escalation in drug use
  • Avoid opioids: mask pain without suppressing pathophysiological mechanism → cognitive impairment or addiction
39
Q

Medication overuse headache

  • Character
  • Cause
  • Mx
A

Character:

→ Gradual ↑headache frequency and drug consumption
→ Change in headache characteristics
→ Ultimately take analgesics and large amounts of caffeine

Causes

daily analgesic use (>10-15d/month) or compound analgesics (esp opiates) and triptans

Mx

Abrupt withdrawal from painkillers or antimigraine drugs

40
Q

Define Trigeminal autonomic cephalalgias (TACs)

3 examples

A

syndromes with combination of facial pain and autonomic dysfunction

□ Cluster headache: severe unilateral periorbital pain of 10min-3h + unilateral autonomic activation
□ Paroxysmal hemicrania: similar to cluster headaches but shorter (2-45min)
□ SUNCT: brief, severe, sharp periorbital pain (15s-3min) a/w conjunctival injection and tearing, ↑by touch or neck movement

41
Q

Cluster headache

  • Pathophysiology
  • Clinical types
  • S/S
A

Pathophysiology: unknown, a/w
Abnormal hypothalamic or thalamic activity
Paroxysmal discharges of central trigeminal and PN pathways

Types:
Episodic: clusters (7-365d) with pain-free remissions (>1mo)
Chronic: recurrent attacks (>1y) without or with pain-free remissions <1mo

S/S:

Headache: extreme unilateral periorbital piercing/throbbing pain

Autonomic features: unilateral lacrimation, nasal congestion, conjunctival injection, sweating ± transient Horner’s syndrome

Agitation

Periodic pain daily with clustering period of pain over days, followed by pain-free periods

42
Q

Management of cluster headache (acute attack and prophylaxis)

A

Acute attacks:
→ SC sumatriptan OR 100% O2 (15L/min) as 1st line
→ Intranasal lidocaine (administered ipsilaterally)
→ PO ergotamine or IV dihydroergotamine (5HT1 agonist)

Prophylaxis: should be started during cluster periods
→ Verapamil
→ Short course oral corticosteroids
→ Other drugs: topiramate, methysergide, gabapentin, Lithium

43
Q

Secondary causes of cluster headache

A

intracranial large artery aneurysms, AVMs, cavernous haemangiomas, meningiomas…

44
Q

Giant cell arteritis

  • Pathophysiology
A

Pathology: subacute granulomatous inflammation of large/medium sized arteries with lymphocyte, plasma cell, neutrophil and giant cell infiltration

□ Results:
→ Thrombosis due to vessel wall thickening:
- Ophthalmic artery → amaurosis fugax
- Basilar artery → posterior circulation infarct
→ Stimulation of nociceptive neurones → pain

□ Site: often involves superficial temporal artery → tender, thickened, non-pulsatile on examination

45
Q

S/S of Giant cell arteritis

A

□ Headache: new onset, bitemporal, intense throbbing headache

□ Neurological S/S:
Stroke, hearing loss, myelopathy, neuropathy
Blindness due to acute ischaemic optic neuropathy (AION)

□ Jaw claudication: pain when chewing or talking due to ischaemia of masseter

□ Visual S/S: amaurosis fugax (transient), can progress into permanent blindness (sight-threatening)
Due to arteritic acute ischaemic optic neuropathy (AAION)

□ Systemic S/S:
Fever, anorexia, malaise
Polymyalgia rheumatica (50%): pain and stiffness over shoulder and pelvic girdle muscles

46
Q

Diagnostic criteria for Giant cell arteritis

A

Diagnostic criteria: ≥3 criteria

(1) Onset ≥50y
(2) New headache
(3) Abnormalities of temporal artery at PE: tender, thickened, non-pulsatile superficial temporal artery
(4) ↑ESR (>50mm/h)
(5) Abnormal findings on biopsy of temporal artery

47
Q

Treatment of Giant Cell Arteritis

A

Tx: urgent prednisolone 60mg qd

□ Urgent Tx prevents blindness and brainstem stroke and ↓headache
□ Parenteral high dose if complications already occurred
□ Gradual ↓dosage to maintenance level according to ESR level

48
Q

Neuralgia

  • Features of pain
  • Temporal course
  • Trigger
A

□ Sudden intense sharp, aching, lancinating, burning, stabbing pain in distribution of nerve
□ Lasts seconds to <2min, occurring repeatedly within short periods
□ Often triggered by sensory/mechanical stimulus

49
Q

Name most frequent neuralgia

S/S

Triggers

Temporal course

A

Trigeminal Neuralgia

S/S: paroxysmal attacks of unilateral severe, short, sharp, stabbing pain

Site: typically unilaterally following V2 or V3 distribution

Triggers: spontaneous or touching a specific spot or doing certain activities (eg. touching/washing face, shaving, brushing teeth, chewing)

Course:
→ Paroxysmal attacks for many times per day, lasting several days or weeks
→ Then stop abruptly followed by pain-free periods for months or years
→ Tend to become more frequent over years with ↓duration of remission periods

50
Q

Causes of trigeminal neuralgia

A

□ Classical TN:
→ Vascular loop compression: most common, 80-90%
→ Idiopathic

□ Other causes (secondary TN):
→ Multiple sclerosis, esp young and when bilateral
→ CPA masses: vestibular neuroma, meningioma, epidermoid cyst, AVM, angiomas…
→ Herpes zoster and post-herpetic neuralgia

51
Q

Treatment of Trigeminal neuralgia

A

Medical Tx: for classic TN
Carbamazepine (first-line, most effective, 75% responsive)

Surgical Tx: for refractory classic TN

  • Peripheral neurectomy, eg. alcohol ablation (temporary relief)
  • Microvascular decompression (separate vessels from trigeminal nerve root)
  • Percutaneous radiofrequency thermocoagulation rhizotomy (artificial lesion for trigger spot on Trigeminal nerve)

Treatment of underlying condition (eg. surgical decompression) for secondary TN

MBBS IV - Junior Clerkship WCS (131 decks)

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